Orthopedics

Radiologic Case Study 

Radiologic Case Study

Prabhakar Rajiah, MBBS, MD, FRCR; Hakan Ilaslan, MD; Murali Sundaram, MD

Abstract

Drs Rajiah, Ilaslan, and Sundaram are from the Imaging Institute, Cleveland Clinic, Cleveland, Ohio.

Drs Rajiah, Ilaslan, and Sundaram have no relevant financial relationships to disclose.

Correspondence should be addressed to: Prabhakar Rajiah, MBBS, MD, FRCR, Imaging Institute, A21, Cleveland Clinic, 9500 Euclid Ave, Cleveland, OH 44195 (radprabhakar@gmail.com).

A 52-year-old woman presented with a 3-month history of left hip pain (Figures 1, 2).

Calcific tendinitis (previously called calcific periarthritis or periarticular apatite deposition disease) is a self-limiting disease caused by the deposition of calcium hydroxyapatite crystals in tendons. It is common in women aged between 30 and 60 years.1 It can affect any tendon of the body. It is usually monoarticular, but polyarticular involvement has been reported.2

Several theories exist on the etiopathogenesis of calcific tendinitis. Initially, degeneration was proposed as a cause, but the acute onset, self-limiting nature, occurrence in viable tissue, and different compositions of calcific salts excludes degeneration as a cause.3 Trauma, endocrine abnormalities, metabolic abnormalities, neurological abnormalities, and extracellular matrix vesicles have also been proposed as etiologies.4 Genetic predilection has been proposed, with increased frequency of HLA-A1 in these patients.5

Calcific tendinitis is currently believed to be a cell-mediated, primary disorder of the tendon that progresses through 4 distinct phases, namely formative, calcific, resorptive, and reparative. In the initial formative phase, a portion of the tendon undergoes chondrocyte mediated fibrocartilagenous transformation in response to hypoxia or mechanical stress. In the earliest stages, there are no radiographic and clinical findings. Subsequently calcific deposits replace the fibrocartilage, progressively enlarge and become chalk-like. In the calcific phase, the disease is quiescent. Well-defined calcification is seen on radiographs. Pain and mechanical symptoms are seen only if the calcification is large. In the resorptive phase, rupturing calcific deposit elicits an inflammatory response surrounding it, with formation of vascularized tissue. The calcification is progressively phagocytosed by macrophages and multinucleated giant cells resembling osteoclasts. The calcification resembles tooth-paste and can leak into adjacent bursal spaces. This is the most painful phase, probably due to increased intratendinous pressure. Radiographs show ill-defined calcification with adjacent soft tissue and occasional bony changes. In the final reparative phase, the calcific deposit is completely phagocytosed. The resultant void in the tendon is replaced by granulation tissue that eventually matures to scar, thus restoring the tendon to its normal state and function.6 Pain may persist until the new collagen fibers are aligned with the long axis of tendon. Radiographs are normal in this phase.3

After the shoulder, the hip is the second most common joint involved in calcific tendinitis. The most common location in the hip is around the greater trochanter, at the insertion sites of the gluteus medius and minimus tendons. Cases have also been reported in the vastus lateralis, pirformis, iliopsoas, adductor magnus, biceps femoris, and gluteus maximus tendons. Rectus femoris is an uncommon site of involvement, with only a few cases reported so far.3 The rectus femoris is an extensor of the leg at the knee and flexor of the thigh. It has a straight head that originates from the anterior inferior iliac spine and a reflected head that originates at the ilium above the acetabulum, both of which are innervated by the posterior division of the femoral nerve (L3, L4).7 The reflected head is more commonly affected by calcific tendinitis than the straight head.8,9

Acute calcific tendinitis of the rectus femoris presents with acute onset pain, typically on the posterolateral aspect of the hip and thigh. The pain may be confused with radicular pain from a prolapsed disk. Due to severe pain, restricted range of motion and limp may be present. Local tenderness, warmth, erythema,…

Drs Rajiah, Ilaslan, and Sundaram are from the Imaging Institute, Cleveland Clinic, Cleveland, Ohio.

Drs Rajiah, Ilaslan, and Sundaram have no relevant financial relationships to disclose.

Correspondence should be addressed to: Prabhakar Rajiah, MBBS, MD, FRCR, Imaging Institute, A21, Cleveland Clinic, 9500 Euclid Ave, Cleveland, OH 44195 (radprabhakar@gmail.com).

The Case:

A 52-year-old woman presented with a 3-month history of left hip pain (Figures 1, 2).

AP Radiograph of the Pelvis.

Figure 1: AP Radiograph of the Pelvis.

Coronal Fat-Suppressed Proton Density-Weighted MRI of the Left Hip.

Figure 2: Coronal Fat-Suppressed Proton Density-Weighted MRI of the Left Hip.

Your diagnosis?

For answer see page 401

Diagnosis:

Calcific Tendinitis of the Rectus Femoris With Intraosseous Extension of Calcification

Answer to Radiologic Case Study

Case facts appear on page 329

A 52-year-old woman presented with a 3-month history of intermittent left hip pain. The pain was worse on squatting, and there was no history of trauma. On examination, the hip had normal alignment. Pain was elicited with combined hip flexion and adduction and with resisted flexion. There was no palpatory pain over the ischial tuberosity, greater trochanter, or anterior inferior iliac spine. There was no flexion contracture. There was 0° to 100° of flexion, internal rotation to 20° in flexion, external rotation to 45° in flexion, abduction to 45°, and adduction to 20°.

Anteroposterior (AP) radiograph of the pelvis showed an ill-defined calcific density (1.8×1.5 cm) in the soft tissue adjacent to the anterior inferior iliac spine. Another smaller calcified density (7×3 mm) was also present in the soft tissue superior to the greater trochanter (Figure 1). The hip joint spaces were maintained. Magnetic resonance imaging (MRI) of the left hip showed calcification in the rectus femoris tendon, adjacent to the anterior inferior iliac spine (Figure 2). There was intraosseous extension of calcification into the anterior inferior iliac spine, with surrounding bone marrow edema (Figures 3, 4). Edema was seen in the rectus femoris tendon surrounding the calcification. In addition, there was a small focus of calcification in the distal gluteus medius tendon at its greater trochanteric insertion, but no intraosseous extension or marrow edema was seen at this location (Figure 5). There was no soft tissue mass or hip joint effusion.

AP Radiograph of the Left Hip Showing a Large Focus of Ill-Defined Calcification Adjacent to the Anterior Inferior Iliac Spine (straight Arrow). There Is Another, Smaller Focus of Well-Defined Calcification Adjacent to the Greater Trochanter (curved Arrow).

Figure 1: AP Radiograph of the Left Hip Showing a Large Focus of Ill-Defined Calcification Adjacent to the Anterior Inferior Iliac Spine (straight Arrow). There Is Another, Smaller Focus of Well-Defined Calcification Adjacent to the Greater Trochanter (curved Arrow).

Proton Density-Weighted, Fat-Suppressed Coronal Image of the Left Hip Showing a Hypointense Calcific Focus (straight Arrow) Extending into the Anterior Inferior Iliac Spine (curved Arrow).

Figure 2: Proton Density-Weighted, Fat-Suppressed Coronal Image of the Left Hip Showing a Hypointense Calcific Focus (straight Arrow) Extending into the Anterior Inferior Iliac Spine (curved Arrow).

Proton Density-Weighted, Fat-Suppressed Coronal Image of the Left Hip Showing a Hypointense Calcific Focus (straight Arrow) Extending into the Anterior Inferior Iliac Spine (curved Arrow). High-Signal Bone Marrow Edema Is Seen in the Anterior Inferior Iliac Spine (arrowhead).

Figure 3: Proton Density-Weighted, Fat-Suppressed Coronal Image of the Left Hip Showing a Hypointense Calcific Focus (straight Arrow) Extending into the Anterior Inferior Iliac Spine (curved Arrow). High-Signal Bone Marrow Edema Is Seen in the Anterior Inferior Iliac Spine (arrowhead).

Proton Density-Weighted, Fat-Suppressed Coronal Image of the Left Hip Showing a Hypointense Calcific Focus Extending into the Anterior Inferior Iliac Spine (curved Arrow). High-Signal Bone Marrow Edema Is Seen in the Anterior Inferior Iliac Spine (arrowhead).

Figure 4: Proton Density-Weighted, Fat-Suppressed Coronal Image of the Left Hip Showing a Hypointense Calcific Focus Extending into the Anterior Inferior Iliac Spine (curved Arrow). High-Signal Bone Marrow Edema Is Seen in the Anterior Inferior Iliac Spine (arrowhead).

Proton Density-Weighted, Fat-Suppressed Coronal Image of the Left Hip Showing a Well-Defined, Hypointense Calcific Focus Adjacent to the Greater Trochanter (straight Arrow).

Figure 5: Proton Density-Weighted, Fat-Suppressed Coronal Image of the Left Hip Showing a Well-Defined, Hypointense Calcific Focus Adjacent to the Greater Trochanter (straight Arrow).

Discussion

Calcific tendinitis (previously called calcific periarthritis or periarticular apatite deposition disease) is a self-limiting disease caused by the deposition of calcium hydroxyapatite crystals in tendons. It is common in women aged between 30 and 60 years.1 It can affect any tendon of the body. It is usually monoarticular, but polyarticular involvement has been reported.2

Several theories exist on the etiopathogenesis of calcific tendinitis. Initially, degeneration was proposed as a cause, but the acute onset, self-limiting nature, occurrence in viable tissue, and different compositions of calcific salts excludes degeneration as a cause.3 Trauma, endocrine abnormalities, metabolic abnormalities, neurological abnormalities, and extracellular matrix vesicles have also been proposed as etiologies.4 Genetic predilection has been proposed, with increased frequency of HLA-A1 in these patients.5

Calcific tendinitis is currently believed to be a cell-mediated, primary disorder of the tendon that progresses through 4 distinct phases, namely formative, calcific, resorptive, and reparative. In the initial formative phase, a portion of the tendon undergoes chondrocyte mediated fibrocartilagenous transformation in response to hypoxia or mechanical stress. In the earliest stages, there are no radiographic and clinical findings. Subsequently calcific deposits replace the fibrocartilage, progressively enlarge and become chalk-like. In the calcific phase, the disease is quiescent. Well-defined calcification is seen on radiographs. Pain and mechanical symptoms are seen only if the calcification is large. In the resorptive phase, rupturing calcific deposit elicits an inflammatory response surrounding it, with formation of vascularized tissue. The calcification is progressively phagocytosed by macrophages and multinucleated giant cells resembling osteoclasts. The calcification resembles tooth-paste and can leak into adjacent bursal spaces. This is the most painful phase, probably due to increased intratendinous pressure. Radiographs show ill-defined calcification with adjacent soft tissue and occasional bony changes. In the final reparative phase, the calcific deposit is completely phagocytosed. The resultant void in the tendon is replaced by granulation tissue that eventually matures to scar, thus restoring the tendon to its normal state and function.6 Pain may persist until the new collagen fibers are aligned with the long axis of tendon. Radiographs are normal in this phase.3

After the shoulder, the hip is the second most common joint involved in calcific tendinitis. The most common location in the hip is around the greater trochanter, at the insertion sites of the gluteus medius and minimus tendons. Cases have also been reported in the vastus lateralis, pirformis, iliopsoas, adductor magnus, biceps femoris, and gluteus maximus tendons. Rectus femoris is an uncommon site of involvement, with only a few cases reported so far.3 The rectus femoris is an extensor of the leg at the knee and flexor of the thigh. It has a straight head that originates from the anterior inferior iliac spine and a reflected head that originates at the ilium above the acetabulum, both of which are innervated by the posterior division of the femoral nerve (L3, L4).7 The reflected head is more commonly affected by calcific tendinitis than the straight head.8,9

Acute calcific tendinitis of the rectus femoris presents with acute onset pain, typically on the posterolateral aspect of the hip and thigh. The pain may be confused with radicular pain from a prolapsed disk. Due to severe pain, restricted range of motion and limp may be present. Local tenderness, warmth, erythema, and positive Ely’s test may be present. Acute phase reactants may be elevated. Tendinitis of the reflected head is more likely to produce acute symptoms due to overlapping of its wide acetabular attachment with the hip joint capsule, which also results in severe restriction of movement.8 Direct head tendinitis presents in nonacute fashion due to increased distance from the joint capsule. However, it can produce painful coxa saltans when impinging against the overlying iliacus muscle.10

Imaging appearances parallel the pathophysiological stages and clinical symptoms.1 In the formative and calcific phases, a well-defined, homogeneous calcific focus is seen adjacent to the anterior inferior iliac spine or acetabulum. Localization to the tendon is identified on the location and comet tail appearance of calcification. Computed tomography (CT) shows well-defined, homogeneous high-density calcific focus within a tendon. On ultrasound, calcification is seen as an echogenic focus, with or without posterior acoustic shadowing. Magnetic resonance imaging shows a calcific focus with low-signal intensity in T1- and T2-weighted sequences, confined to a tendon. Formative and calcific phases are asymptomatic except for large calcifications, which can produce pain or mechanical symptoms. Differential diagnoses of this radiographic appearance may include avulsion fracture, os acetabuli, sesamoid bone, myositis ossificans, and surface malignancies.

In the acutely symptomatic resorptive phase, the radiograph shows ill-defined, amorphous, fluffy calcification. Computed tomography shows ill-defined, heterogeneous calcification reflecting its semi-liquid nature. Radiographs and CT may show adjacent osseous changes like erosion, periosteal reaction, and soft tissue calcification.3 Magnetic resonance imaging may show the erosion, intraosseous extension, and edema in tendon, soft tissue, and bone marrow. Differential diagnosis for the clinical presentation includes septic arthritis, stress fracture, muscle strain or rupture, arthritis, neoplasm, and myositis ossificans. The presence of calcification and other changes confined to a tendon is a characteristic feature. Absence of joint effusion lowers the suspicion of septic arthritis. Absence of soft tissue mass excludes a neoplasm.3

Although calcific tendinitis is not uncommon in the population, intraosseous extension is uncommon. Osseous involvement is more commonly seen at the proximal linea aspera of the femur and the anterior proximal humerus. Cortical erosion is the most common finding in osseous involvement (78%), representing calcium deposition and hypervascularity induced by local inflammation. Periosteal reaction is also caused by local inflammatory response. Marrow involvement is seen in 36% of intraosseous extension and is difficult to appreciate on radiographs. Reactive edema without intraosseous extension has also been reported. Osseous involvement is underestimated in radiographs and is best seen in tangential radiographs of cortex. Computed tomography is more sensitive for osseous changes, and MRI is more sensitive for marrow changes.11

Radiographs are often adequate for making the diagnosis and are the most commonly used modality. In indeterminate cases, MRI can be used in the evaluation of soft tissue abnormalities and intraosseous extension. It can also evaluate for other causes of hip pain. Computed tomography may be used for localizing the calcification to a tendon, particularly in unusual places and for further evaluation of osseous abnormalities such as erosion, periosteal reaction, and soft tissue calcification. It is also the most accurate technique in assessing the consistency of calcification, which may be useful in determining the optimal therapy.3 Ultrasound can also demonstrate calcification but cannot assess its consistency or associated osseous and soft tissue changes, and hence is not routinely used in the hip. In cases where MRI is the initial imaging modality, the findings should be correlated with radiographs to confirm calcification and avoid misinterpretation as neoplasm, infection, or arthritis.

Calcific tendinitis should be in the differential diagnosis of discrete cortical erosions at sites of tendinous insertions, even if the radiograph does not show calcifications, since occasionally calcification may be rapidly resorbed, leaving only the defect.11 Bilateral symmetrical involvement is another clue. Imaging helps in avoiding unnecessary aspiration or biopsy. Even if biopsy is performed in indeterminate cases, the pathologist should be aware of the radiologic suspicion of calcific tendinitis to avoid misinterpretation of chondroid metaplasia of calcific tendinitis as a chondroid neoplasm.4

Treatment

Due to its self-limiting nature, calcific tendinitis is usually managed conservatively with rest, nonsteroidal anti-inflammatory drugs, heat/cold, and physical therapy. Invasive options are used when conservative therapy fails or if symptoms are severe in the acute phase. Aspiration, perforation and lavage, and/or injection of steroids and local anesthetics under fluoroscopy,8 ultrasound,12,13 or CT9 guidance have been shown to provide symptomatic relief and resolution of calcification in the majority of these cases with a low complication rate.8,12 Extracorporeal lithotripsy,14 arthroscopy, and surgery can also be performed in recalcitrant cases. Ultrasound therapy and acetic acid iontophoresis have not been shown to be effective.15

Conclusion

Radiographs are useful in the diagnosis and characterization of calcific tendinitis in the rectus femoris, an uncommon cause of hip pain. Aggressive osseous changes may occasionally be seen, as in the case illustrated here, which should not be confused with neoplasm or infection. Demonstration of the calcific deposits and osseous or soft tissue changes localized to rectus femoris tendon on radiographs, CT, or MRI helps in making the diagnosis and avoids unnecessary aspiration and biopsies. Misdiagnosis leads to inappropriate treatment and delayed recovery.

References

  1. Uhthoff HK. Calcifying tendinitis. Ann Chir Gynaecol. 1996; 85(2):111–115.
  2. Cannon RB, Schmid FR. Calcific periarthritis involving multiple sites in identical twins. Arthritis Rheum. 1973; 16(3):393–396. doi:10.1002/art.1780160316 [CrossRef]
  3. Kraemer EJ, El-Khoury GY. Atypical calcific tendinitis with cortical erosions. Skeletal Radiol. 2000; 29(12):690–696. doi:10.1007/s002560000278 [CrossRef]
  4. Siegal DS, Wu JS, Newman JS, Del Cura JL, Hochman MG. Calcific tendonitis: a pictorial review. Can Assoc Radiol J. 2009; 60(5):263–272. doi:10.1016/j.carj.2009.06.008 [CrossRef]
  5. Sengar DP, McKendry RJ, Uhtoff HK. Increased frequency of HLA-A1 in calcifying tendinitis. Tissue Antigens. 1987; 29(3):173–174. doi:10.1111/j.1399-0039.1987.tb01571.x [CrossRef]
  6. Uhthoff HK, Loehr JW. Calcific tendinopathy of the rotator cuff: pathogenesis, diagnosis, and management. J Am Acad Orthop Surg. 1997; 5(4):183–191.
  7. Yun HH, Park JH, Park JW, Lee JW. Calcific tendinitis of the rectus femoris. Orthopedics. 2009; 32(7). doi: doi:10.3928/01477447-20090527-13 [CrossRef] .
  8. Sarkar JS, Haddad FS, Crean SV, Brooks P. Acute calcific tendinitis of rectus femoris. J Bone Joint Surg Br. 1996; 78(5):814–816.
  9. Pierannunzii L, Tramontana F, Gallazzi M. Case report: calcific tendinitis of the rectus femoris: a rare cause of snapping hip [published online ahead of print January 7, 2010]. Clin Orthop Relat Res. 2010; 468(10):2814–2818. doi:10.1007/s11999-009-1208-9 [CrossRef]
  10. Uhthoff HK, Sarkar K. Calcifying tedinitis. Baillieres Clin Rheumatol. 1989; 3(3):567–581. doi:10.1016/S0950-3579(89)80009-3 [CrossRef]
  11. Flemming DJ, Murphey MD, Shekitka KM, Temple HT, Jelinek JJ, Kransdorf MJ. Osseous involvement in calcific tendinitis: a retrospective review of 50 cases. AJR Am J Roentgenol. 2003; 181(4):965–972.
  12. Braun-Moscovici Y, Schapira D, Nahir AM. Calcific tendinitis of the rectus femoris. J Clin Rheumatol. 2006; 12(6):298–300. doi:10.1097/01.rhu.0000249896.43792.62 [CrossRef]
  13. De Zordo T, Ahmad N, Ødegaard F, et al. US-guided therapy of calcific tendinopathy: clinical and radiological outcome assessment in shoulder and non-shoulder tendons [published online ahead of print April 22, 2010]. Ultraschall Med. 2011; 32(Suppl 1):S117–123. doi:10.1055/s-0029-1245333 [CrossRef]
  14. Oh KJ, Yoon JR, Shin DS, Yang JH. Extracorporeal shock wave therapy for calcific tendinitis at unusual sites around the hip. Orthopedics. 2010; 33(10). doi: doi:10.3928/01477447-20100826-30 [CrossRef] .
  15. del Cura JL, Torre I, Zabala R, Legórburu A. Sonographically guided percutaneous needle lavage in calcific tendinitis of the shoulder: short and long-term results. AJR Am J Roentgenol. 2007; 189(3):W128–134. doi:10.2214/AJR.07.2254 [CrossRef]

Enhance your diagnostic skills with this “test yourself” monthly column, which features a radiograph and challenges you to make a diagnosis.

Authors

Drs Rajiah, Ilaslan, and Sundaram are from the Imaging Institute, Cleveland Clinic, Cleveland, Ohio.

Drs Rajiah, Ilaslan, and Sundaram have no relevant financial relationships to disclose.

Correspondence should be addressed to: Prabhakar Rajiah, MBBS, MD, FRCR, Imaging Institute, A21, Cleveland Clinic, 9500 Euclid Ave, Cleveland, OH 44195 (radprabhakar@gmail.com).

10.3928/01477447-20110317-32

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